The role and control of the capacity vessels in the maintenance of cardiovascular homeostasis is the long-range objective of this project. The immediate objective is to measure the range of active venoconstriction between the fully relaxed capacity vessels and those maximally contracted. Tissues to be studied include small intestine, gracilis muscle, liver and spleen of dogs. We will further evaluate and develop the method of measuring vascular volume based on the mean-transit-time of an indicator and the rate of flow. Constant indicator infusion will be used rather than a slug injection. The importance of passive changes in vascular volume due to changes in flow and thus transmural pressure will be studied. The time course of changes in vascular volume resulting from changes in venous pressure or perfusion rate will also be considered in partitioning dynamic changes in capacity vessel compensation between passive elastic, visco-elastic, and active smooth muscle effects. Simulation techniques will eventually be used to summarize the data. Because the interaction between the blood volume and the capacity vessels is important in determining venous return, cardiac filling and so cardiac output, the capacity vessel dynamics are important in recovery from hemorrhage and shock and might be part of the etiology of hypertension. BIBLIOGRAPHIC REFERENCES: Rothe, C. F. and J. A. Drees. Vascular capacitance and fluid shifts in dogs during prolonged hemorrhagic hypotension. Circ. Res. 38:347-356, May, 1976. Rothe, C. F. Reflex vascular capacity reduction in the dog. Circ. Res., November 1976 (in press).